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Published on: June 12, 2019
High serum pentosidine in branch atheromatous disease among small vessels occlusion
Toshiki Ikeda1,2, Keisuke Maruyama3, Nobuyuki Ito3,4
1Department of Cerebrovascular Surgery and Stroke Center, International Medical Center, Saitama Medical University, Saitama, Japan - schwein0920@me.com.
Insights
High serum pentosidine levels are linked to cerebral branch atheromatous disease (BAD), a condition causing worse outcomes in acute ischemic stroke patients. This finding aids in distinguishing BAD from lacunar infarction.
Area of Science:
- Neurology
- Vascular Medicine
- Biochemistry
Background:
- Cerebral branch atheromatous disease (BAD) is associated with poorer stroke progression and neurological decline compared to lacunar infarction.
- Advanced glycation end products, such as pentosidine, are implicated in atherosclerosis and plaque progression.
- The relationship between serum pentosidine and small vessel occlusion, particularly BAD, remains underexplored.
Purpose of the Study:
- To investigate the association between serum pentosidine levels and cerebral branch atheromatous disease (BAD) in patients with acute ischemic stroke.
- To determine if serum pentosidine can differentiate BAD from lacunar infarction.
- To identify serum pentosidine as an independent risk factor for BAD.
Main Methods:
- Serum pentosidine levels were measured in 56 acute ischemic stroke patients (21 BAD, 35 lacunar).
- Univariate and multivariate logistic regression analyses were employed to assess risk factors, including pentosidine.
- Sensitivity and specificity of pentosidine for discriminating BAD from lacunar infarction were calculated.
Main Results:
- Serum pentosidine levels were significantly higher in the BAD group (0.081±0.081 µg/mL) compared to the lacunar group (0.046±0.043 µg/mL) (P<0.05).
- High serum pentosidine was significantly related to BAD in univariate analysis (P=0.01).
- Multivariate analysis identified high serum pentosidine as the sole independent risk factor for BAD (P=0.03), with 90% sensitivity and 44% specificity.
Conclusions:
- Elevated serum pentosidine levels in the acute phase of stroke are associated with cerebral branch atheromatous disease (BAD).
- High pentosidine levels correlate with a worse outcome in patients experiencing small vessel occlusion.
- Serum pentosidine may serve as a valuable biomarker for identifying BAD and predicting stroke outcomes.
Background:
Cerebral branch atheromatous disease (BAD) are more likely to experience progressing stroke and neurological deterioration compared with lacunar infarction, although these small vessels occlusions are difficult to discriminate in acute phase of ischemic stroke. Advanced glycation end products including pentosidine have been implicated in atherosclerosis, and were associated with atheroma plaque progression. However, little is known about a relationship between serum pentosidine and small vessels occlusion.
Methods:
Serum pentosidine levels were measured in 56 patients (BAD: N.=21; lacunar: N.=35) with small vessels occlusion among consecutive 208 patients with acute ischemic stroke at initial hospitalization as well as other risk factors of stroke. Univariate and multivariate logistic regression analyses were performed to analyze relationship between risk factors including pentosidine and small vessels occlusion. Sensitivity and selectivity of pentosidine to discriminate BAD from lacunar were calculated.
Results:
Serum pentosidine was significantly higher in BAD group than lacunar group (0.081±0.081 µg/mL and 0.046±0.043 µg/mL, P<0.05). In the univariate logistic regression analyses, BAD was significantly related to high serum pentosidine (P=0.01), absence of dyslipidemia (P=0.04), and worse outcome measured by modified Rankin Scale (P=0.03). Multivariate logistic regression analysis showed that only high level of serum pentosidine was the independent risk factor for BAD (P=0.03). Sensitivity and specificity were 90% and 44%, respectively.
Conclusions:
High level of serum pentosidine in acute phase of stroke was associated with BAD, which led to worse outcome among patients with small vessels occlusion.
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